Intracellular sensing of viral genomes and viral evasion

During viral infection, virus-derived cytosolic nucleic acids are recognized by host intracellular specific sensors. The efficacy of this recognition system is crucial for triggering innate host defenses, which then stimulate more specific adaptive immune responses against the virus. Recent studies show that signal transduction pathways activated by sensing proteins are positively or negatively regulated by many modulators to maintain host immune homeostasis. However, viruses have evolved several strategies to counteract/evade host immune reactions. These systems involve viral proteins that interact with host sensor proteins and prevent them from detecting the viral genome or from initiating immune signaling. In this review, we discuss key regulators of cytosolic sensor proteins and viral proteins based on experimental evidence.
Viral infection: Evasion strategies subvert antiviral defenses Viruses escape the body’s immune surveillance mechanisms by manipulating and subverting key intracellular sensors of viral RNA or DNA. In a review article, Jong-Soo Lee and colleagues from Chungnam National University in Daejeon, South Korea, discuss the strategies used by viral pathogens to avoid detection by immune receptors or to block activation of these receptors and the associated signaling molecules, thus preventing expression of antiviral genes. These strategies include modifying viral nucleic acids or making them inaccessible, and interference with sensor proteins, either though degradation, altered processing or relocalization within the cell. The authors summarize rapid advances in scientists’ understanding of sensor-mediated antiviral responses at the molecular level, and highlight how that knowledge could help guide the development of novel vaccines and antiviral agents.